Nicotinic acetylcholine receptor interaction with beta-amyloid: molecular, cellular, and physiological consequences.

Elevated amyloid-beta peptide (Abeta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery of an Abeta - nAChR interaction, much effort has been expended to characterize the consequences of high versus low concentrations of Abeta on nAChRs. This review will discuss current knowledge on the subject at the molecular, cellular, and physiological levels with particular emphasis on understanding how Abeta - nAChR interaction may contribute to normal physiological processes as well as the etiology of AD.